Abstract
The role of the Human Immunodeficiency Virus (HIV) in the pathogenesis of the Acquired Immune-Deficiency Syndrome (AIDS) is changed. Direct HIV-mediated killing of CD4+ T cells is not the only mechanism leading to lymphocyte depletion. There is increasing evidence that, during the chronic phases of infection, T cell activation, accelerated cell turnover, and cytokines imbalance induce the so-called cell cycle dysregulation (CCD). CCD is a recently discovered immune-pathogenic mechanism that mainly induces the depletion of both CD4+ and CD8+ uninfected T cells. It is due to a significant perturbation of protein metabolism as ubiquitin pathway defects of protein degradation are associated with an increased and unscheduled expression of cyclin B and p34 cdc kinase. Moreover, significant changes in the nucleolar structure and post-translational regulation of nucleolin have also been described. As modulation of CCD by anti-retroviral and immune-therapies has been suggested to predict a good immunological response in HIV-infected patients, a better understanding of such a mechanism is needed in order to further clarify its role in the pathogenesis and progression of HIV infection.
Keywords: Cell cycle dysregulation, cyclin B, apoptosis, HIV infection
Current Medicinal Chemistry
Title: New Insights on the Perturbations of T Cell Cycle During HIV Infection
Volume: 14 Issue: 18
Author(s): Domenico Galati and Marialuisa Bocchino
Affiliation:
Keywords: Cell cycle dysregulation, cyclin B, apoptosis, HIV infection
Abstract: The role of the Human Immunodeficiency Virus (HIV) in the pathogenesis of the Acquired Immune-Deficiency Syndrome (AIDS) is changed. Direct HIV-mediated killing of CD4+ T cells is not the only mechanism leading to lymphocyte depletion. There is increasing evidence that, during the chronic phases of infection, T cell activation, accelerated cell turnover, and cytokines imbalance induce the so-called cell cycle dysregulation (CCD). CCD is a recently discovered immune-pathogenic mechanism that mainly induces the depletion of both CD4+ and CD8+ uninfected T cells. It is due to a significant perturbation of protein metabolism as ubiquitin pathway defects of protein degradation are associated with an increased and unscheduled expression of cyclin B and p34 cdc kinase. Moreover, significant changes in the nucleolar structure and post-translational regulation of nucleolin have also been described. As modulation of CCD by anti-retroviral and immune-therapies has been suggested to predict a good immunological response in HIV-infected patients, a better understanding of such a mechanism is needed in order to further clarify its role in the pathogenesis and progression of HIV infection.
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Cite this article as:
Domenico Galati and Marialuisa Bocchino , New Insights on the Perturbations of T Cell Cycle During HIV Infection, Current Medicinal Chemistry 2007; 14 (18) . https://dx.doi.org/10.2174/092986707781368559
DOI https://dx.doi.org/10.2174/092986707781368559 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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